pubmed-article:20969596 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20969596 | lifeskim:mentions | umls-concept:C0018894 | lld:lifeskim |
pubmed-article:20969596 | lifeskim:mentions | umls-concept:C1521991 | lld:lifeskim |
pubmed-article:20969596 | lifeskim:mentions | umls-concept:C1420610 | lld:lifeskim |
pubmed-article:20969596 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:20969596 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:20969596 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:20969596 | pubmed:dateCreated | 2010-10-25 | lld:pubmed |
pubmed-article:20969596 | pubmed:abstractText | Current research suggests that a number of newly identified T-helper cell subsets retain a degree of context-dependent plasticity in their signature cytokine expression patterns. To understand this process, a major challenge is to determine the molecular mechanisms by which lineage-defining transcription factors regulate gene expression profiles in T-helper cells. This mechanistic information will aid in our interpretation of whether a T-helper cell state that expresses or retains the capacity to re-express a combination of lineage-defining transcription factors will have a stable or more flexible gene expression profile. Studies examining the developmental T-box transcription factor T-bet demonstrate the powerful information that is gained from combining in vivo analysis with basic biochemical and molecular mechanism approaches. Significantly, T-bet's ability to physically recruit epigenetic modifying complexes, in particular a Jmjd3 H3K27-demethylase and a Set7/9 H3K4-methyltransferase complex, to its target genes allows T-bet to effectively reverse and establish new epigenetic states. This observation suggests that until T-bet is permanently extinguished, T-helper cells will retain some plasticity toward a T-helper 1-like program. Therefore, insight into the complexity of T-helper cell commitment decisions will be aided by determining the molecular mechanisms for lineage-defining transcription factors. | lld:pubmed |
pubmed-article:20969596 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20969596 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20969596 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20969596 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20969596 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20969596 | pubmed:language | eng | lld:pubmed |
pubmed-article:20969596 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20969596 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:20969596 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20969596 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20969596 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20969596 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20969596 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20969596 | pubmed:month | Nov | lld:pubmed |
pubmed-article:20969596 | pubmed:issn | 1600-065X | lld:pubmed |
pubmed-article:20969596 | pubmed:author | pubmed-author:WeinmannAmy... | lld:pubmed |
pubmed-article:20969596 | pubmed:author | pubmed-author:MillerSara... | lld:pubmed |
pubmed-article:20969596 | pubmed:copyrightInfo | © 2010 John Wiley & Sons A/S. | lld:pubmed |
pubmed-article:20969596 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20969596 | pubmed:volume | 238 | lld:pubmed |
pubmed-article:20969596 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20969596 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20969596 | pubmed:pagination | 233-46 | lld:pubmed |
pubmed-article:20969596 | pubmed:dateRevised | 2011-11-1 | lld:pubmed |
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pubmed-article:20969596 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20969596 | pubmed:articleTitle | Molecular mechanisms by which T-bet regulates T-helper cell commitment. | lld:pubmed |
pubmed-article:20969596 | pubmed:affiliation | Molecular and Cellular Biology Program, University of Washington, Seattle, WA, USA. | lld:pubmed |
pubmed-article:20969596 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20969596 | pubmed:publicationType | Review | lld:pubmed |
pubmed-article:20969596 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:20969596 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |